This invention relates generally to the field of endovascular, thoracic and urological surgery, and relates to catheter balloon delivery stent procedures in particular. Over the last several decades, the treatment of vascular congestion and urological constrictions has been revolutionized by percutaneous balloon angioplasty methods and advances in catheter construction and treatment, which allow a surgeon to insert a simple catheter device along a blood vessel or urethra and surgically shave or mechanically expand the inner wall of the vessel or tubular organ where desired. Such procedures in most instances involve less risk than open surgery, and have proven effective in a wide range of circumstances. However, balloon angioplasty procedures involve some trauma to the vessel wall and this injury may trigger a complex sequence of cellular responses that in many cases lead to restenosis, or closing off, of the treated portion. Studies have reported incidences of restenosis as high as 35-50% following percutaneous transluminal angioplasty of coronary vessels, and incidence of 19-30% after treatment of peripheral lesions. It is therefore an active and major area of medical research to find methods and treatment devices which inhibit or prevent such restenosis.
Uncontrolled cellular proliferation and other factors such as migration of smooth muscle cells into surrounding tissue, and extracellular matrix production by proliferating cells have all been identified as factors which may contribute to the processes of restenosis. Thus, inhibiting any of these three factors may prove effective in preventing the restenosis or short term closing off of a dilated or recanaled vessel following balloon dilation.
The strategies for effecting such inhibition have evolved in three general classes. The first of these is to place a porous, radially expanding metal stent into the affected area to mechanically xe2x80x9chold openxe2x80x9d the vessel or tubular organ. Another method involves placing an expandable barrier structure in combination with a stent within the vessel to seal off the inner surface tissue to minimize restenosis. The third strategy involves delivering treatment or medication locally to the affected regions of tissue in the vessel to inhibit stenotic growth processes.
Vascular stents of the first-mentioned class, such as those described and publicized by Palmaz offer good results in mechanically keeping a vessel open for a period of time. However, recent studies have shown that due to the large percentage of open surface or through-openings of these balloon-expanded or self-expanded stents, the same diseased cells which caused the stenotic lesion orginally readily proliferate through the open stent structure, causing restenosis of the stented vessel. This process of restenosis has been reported to occur in three stages, or phases, as follows:
Various devices have been used or proposed, including porous balloons which are advanced along the vessel to the position of the region to be treated, or hydrogel-coated balloons. Delivery of material to the vessel wall has been enhanced by providing material sandwiched between an inner balloon and an outer porous balloon, so that inflation of the inner balloon ejects medication through the pores of the outer balloon against the vessel lining.
Among purely physical techniques for endoluminal treatment, there have long existed devices such as that shown in U.S. Pat. No. 4,562,596, wherein a thin lining is secured within the vessel to strengthen the wall and prevent aneurysm. Such lining may also act as a barrier against spread of tissue from the covered region of the wall, preventing migration along the vessel or into the bloodstream. Other techniques have been proposed, such as that of the published international application WO9404096 which involves unfurling a reinforced rolled sheet to radially expand it into a shape-retaining tube liner or stent, and that of U.S. Pat. No. 5,316,023 which involves expanding a web-like tubular structure within a vessel. The web-like structure is embedded in an expandable plastic material, which apparently relies on the embedded web for shape retention.
In addition to the foregoing approaches, localized drug delivery has been achieved by periadventitial deposition of an active agent to exploit local diffusion as the primary delivery mechanism. For example, heparin in a matrix material placed in the periadventitial space of arteries following injury has been shown to reduce neointima formation in the first week. Provision of materials in a silastic shell has also been found to be an effective mechanism of drug delivery.
While indwelling vascular liners may prove effective for control of tissue proliferation conditions and restenosis, the implementation of an endoprosthetic liner to be delivered percutaneously poses severe problems due to constraints of size necessary for inserting such a device, and of strength and uniformity necessary to undergo sufficient expansion from a small diameter. While the techniques of catheterization have been developed with much technological detail for the delivery of balloons, for taking of samples, and for the performance of mapping or ablation functions in cardiac tissue, the delivery and installation of a vascular liner would pose unique problems because its operation requires its final diameter to match that of the vessel. An angioplasty balloon is generally formed of highly non-elastic material which is inflated to a high positive pressure to a maximum, fixed, dilated outer diameter. Such balloons are inflated only temporarily to enlarge the stenotic area of the vessel. Pumping balloons for cardiac assistance need not exert such great forces and may be formed with much thinner walls, allowing them to be folded or wrapped to reduce their size and to achieve a small diameter for insertion.
A conventional vascular liner, on the other hand, has a resting state diameter equal to or about ten percent greater than the inner diameter of the vessel in which it is to reside. In order to advance a conventional vascular, graft intraluminally, particularly within small branching vessels to the site of application, it is necessary that it be rolled, folded, or otherwise made much smaller in order to pass through tortuous or disease-affected regions of the vessel.
Accordingly, it would be desirable to provide a vascular liner of enhanced utility to inhibit restenosis and having a small ratio of insertion diameter to expanded diameter.
It is also desirable to provide a vascular liner which is sufficiently compact for intraluminal insertion and installation, yet after insertion and installation maintains a uniform and functional cellular barrier membrane function with dimensional stability and strength.
These and other features of the invention are achieved in a method of treatment wherein a plastic vessel liner is inserted within a vessel by placement onto an insertion catheter and in an endovascular liner assembly. The catheter is moved into position within the stenotic region under fluoroscopy and the vascular liner is then radially expanded along with an expandable rigidified stent, all in one step to fit an affected site in the vessel or tubular organ. The small OD tubular liner has a hollow center lumen sufficiently large to house a radial expanding stent and inflation balloon, and has a generally cylindrical shape and a length equal to a selected treatment interval along the vessel. Its initial or resting state diameter is substantially less than the inner diameter of the vessel in which it is to be inserted. Once inserted to the desired site within a vessel, the liner is deformed by expanding it beyond its limit of plastic deformation to enlarge the liner. This simultaneously develops or enhances porosity in the liner which, as discussed further below, may be tailored in any of several ways to achieve a desired set of controlled tissue growth, controlled material delivery or controlled growth inhibition characteristics. Once fixed in place by the expanded inner stent, the insertion catheter is then withdrawn, leaving the expanded liner fitted in position on the outside of the stent within the vessel. The liner may be expanded using a radially expandable stent, such as a porous stainless steel tube of Palmaz type, or using a helical or crossed-helical wire mesh stent that expands radially. Alternatively, an angioplasty balloon or specially shaped balloon may be fitted within the liner and may simply be inflated to stretch the liner and alter its size and porosity. In this case, a separate stent or anchor ring may be provided as a secondary step to secure at least one end of the expanded liner after the balloon is withdrawn.
Preferably the liner on the outside of the stent is made of a polytetrafluoroethylene (PTFE) or similar fluoropolymer, which most preferably is formed in a tubular shape by extrusion at high pressure of a paste consisting of powder material with a lubricant or extrusion aid, such as Isopar or other mineral spirit. Following extrusion, the tube may be stretched in a direction along its axis, by a factor of between approximately 2 and 10 to develop a microporous structure consisting of circumferentially-extending nodes, or solid fragments with radially-extending interstitial spaces between the nodes. The interstitial spaces are filled with a multitude of thin connective fibrils, which allow relatively unhindered fluid and gas communication radially through the wall of the liner. Preferably the PTFE material has a nodal structure in which relatively large nodes extending 100 to 1000 micrometers in a radial direction, and most preferably extending between 200-500 micrometers radially, and extending 100-1000 micrometers or more in a circumferential direction is used, as described for example in the aforesaid commonly owned U.S. patents which are hereby incorporated by reference. This large nodal structure enables the liner to stretch by a factor of 5 to 10 times without membrane rupture. This axially-stretched PTFE material has negligible Poisson coupling, so that when the liner is expanded radially, the forces in the axial and circumferential directions of the sheet do not couple very strongly, and it does not shorten by any appreciable amount in length, while it may be expanded by a factor of two or more in radius. This radial expansion of the liner does result in a slight thinning of its wall, in addition to radial stretching of the circumferentially oriented nodal structure of the PTFE material therein. The expanded liner thus maintains a nearly equivalent pore structure to that originally possessed by the unexpanded liner.
After balloon/stent expansion, the angioplasty balloon (if the expansion has been performed by balloon) is deflated and withdrawn, leaving the expanded liner in place, supported by an internal expanded stent or support. A plastic or wire snap expansion ring or similar stent device may be placed as a secondary step to internally secure the liner at both its upstream end and downstream ends tightly against the inner surface of the diseased vessel wall as an alternative to a one-step balloon/stent insertion technique. Preferably, a fully supporting stent is used, to prevent leakage and accumulation of fluid between the liner and the vessel wall. Also, a vessel liner can be placed onto an expandable stent as a one-piece assembly by which a balloon catheter dictates or expands both the sent and liner simultaneously, and the catheter may be disengaged or deflated leaving the stent and liner to remain fixed in place securely against the vessel wall after the delivery catheter has been withdrawn.